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UCSF Institute for Neurodegenerative Diseases

The Institute for Neurodegenerative Diseases (IND) is a research institute inside the University of California San Francisco, not a separate legal body and not a clinic. It occupies the third floor of the Sandler Neurosciences Center at the UCSF Mission Bay campus in San Francisco. Stanley Prusiner, who discovered prions and received the 1997 Nobel Prize, founded it in the late 1990s (1998 in a UCSF announcement, 1999 in a recruitment profile) and directed it until 30 June 2026. Since 1 July 2026 Jason Gestwicki has been interim director while UCSF runs a national search, and Prusiner remains on the faculty with a laboratory that UCSF says will focus on Parkinson disease therapies. The stated mission is drugs that stop prion accumulation, read broadly: most recent output treats Alzheimer, Parkinson, multiple system atrophy and tauopathies as prion disorders and works on tau and alpha-synuclein filament structures, imaging and models. Classical prion disease is the historical root (the 2-aminothiazole antiprion compounds, the synthetic strain work and a role in the UCSF quinacrine trial in sporadic CJD), but on the pages opened recent work directly on CJD or genetic prion disease is limited to a 2023 anle138b mouse study. Long-running NIA program funding to Prusiner ended in March 2025. The institute offers no patient service.

Key facts

  • The IND is a unit of UCSF at 675 Nelson Rising Lane, third floor, Sandler Neurosciences Center, Mission Bay, San Francisco; its public contact is an institutional phone number and email, and it describes its work as research and drug discovery toward molecular diagnostics and treatments for neurodegenerative disease.
  • Its stated overarching goal is drugs that stop prion accumulation and so halt neurodegeneration, with Alzheimer, Parkinson, CJD and dementia after traumatic brain injury named as targets.
  • Stanley Prusiner is listed as Founding Director; he is Professor of Neurology and Biochemistry, discovered prions and received the 1997 Nobel Prize, and his current research aims at therapeutics that reduce specific prions in Alzheimer, Parkinson, MSA, FTD, CTE and CJD.
  • Prusiner stepped down as director effective 30 June 2026, staying on the faculty with an active laboratory; Jason Gestwicki has served as interim director since 1 July 2026 while a national search is conducted, and the IND leadership page already shows Gestwicki as Interim Director.
  • The leadership page lists six principal investigators (Condello, Gestwicki, Kampmann, Mordes, Prusiner, Southworth), a drug discovery lead for prion biology (Jacob Ayers), and its own animal facility director.
  • The best documented antiprion drug programme is the 2-aminothiazole series such as IND24, which extended survival in mice infected with mouse-adapted and deer and elk CWD prions but showed no benefit against sporadic CJD prions in humanized mice, and selected drug-resistant prions.
  • IND researcher George Carlson co-authored a February 2023 NINDS-funded study with McLaughlin Research Institute and Broad Institute scientists testing anle138b in mouse models of genetic prion disease (D178N and E200K), which found that the genetic models lacked clear disease endpoints for drug testing.
  • The IND lists among its publications the UCSF quinacrine trial in sporadic CJD led by Michael Geschwind of the Memory and Aging Center with Prusiner as a co-author; the trial was UCSF-sponsored with NIA as collaborator, ran from April 2005 to June 2012 and randomized 51 people.
  • Recent output is dominated by tau, amyloid beta and alpha-synuclein prion work: an October 2024 JAMA Neurology opinion by Condello, Westaway and Prusiner on extending the prion paradigm to Alzheimer and Parkinson disease, cryo-EM structures of MSA and Lewy body alpha-synuclein filaments, and tau prions in transgenic rats.
  • Funding is mainly federal and philanthropic: Prusiner held NIA program project P01AG002132 from 1981 to March 2025, with no later NIH award shown on his profile; other IND faculty hold foundation awards such as Thome, Ludwig and the Sandler Program for Breakthrough Biomedical Research, and the Gestwicki laboratory is part of a 32.3 million dollar, five-year Hevolution Foundation consortium announced on 10 June 2024.
  • The CJD Foundation funded IND work directly: the 2016 Robert Dodd Memorial grant went to Zuzana Krejciova at the IND for human stem cell derived neural models of sporadic CJD prion propagation and drug discovery.
  • The institute offers no clinical, diagnostic or referral service to patients or families; its prion disease page is an educational overview and the public routes are contact details, a giving page and a community committee.

Timeline

  1. 1997Prusiner receives the Nobel Prize in Physiology or Medicine for the discovery of prions.
  2. 1998IND founded by Prusiner per the UCSF School of Medicine announcement; a recruitment profile gives 1999.
  3. 2012UCSF quinacrine trial in sporadic CJD completed, after starting in April 2005.
  4. 2015Prusiner laboratory papers on IND24 report efficacy against CWD prions but not sporadic CJD prions in humanized mice.
  5. 2016CJD Foundation Robert Dodd Memorial grant to Zuzana Krejciova at the IND for stem cell models of sporadic CJD.
  6. 2023J Virol trial of anle138b in mouse models of genetic prion disease with Carlson of the IND and the McLaughlin Research Institute.
  7. 2024IND announces the Gestwicki laboratory share in a 32.3 million dollar Hevolution Foundation proteostasis consortium.
  8. 2024JAMA Neurology opinion by Condello, Westaway and Prusiner on extending the prion paradigm to Alzheimer and Parkinson disease.
  9. 2025NIA program project P01AG002132, held by Prusiner since 1981, ends.
  10. 2025J Mol Biol corrigendum on the IND synthetic prion strain paper, crediting four NIA awards.
  11. 2026Prusiner steps down as IND director after nearly three decades and remains on the faculty.
  12. 2026Jason Gestwicki becomes interim director while a national search runs.
  13. 2026bioRxiv preprint from Ayers, Prusiner and colleagues on infectious low-twist alpha-synuclein filaments in Lewy bodies.
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